Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.1.7 (acetylcholinesterase)
28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The organization of the thalamostriatal projections arising from the centromedian (CM) and parafascicular (Pf) thalamic nuclei in the squirrel monkey (Saimiri sciureus) was studied at both light and electron microscopic levels. Following selective injections of the anterograde axonal tracer Phaseolus vulgaris-leucoagglutinin (PHA-L) into the CM or Pf, patterns of terminal arborization within the striatum were compared to the biochemical heterogeneity of the striatum as revealed by immunohistochemical staining for the calcium-binding protein calbindin D-28k (CaBP), and histochemical staining for the enzymes acetylcholinesterase (AChE) and nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-diaphorase). The PHA-L-labeled axon terminals within the striatum were further analyzed at the ultrastructural level to characterize their pattern of synaptic organization. Dense and heterogeneous terminal fields occur in the "sensorimotor" territory of the striatum after CM injections, or in the "associative" striatal territory following Pf injections. In the associative territory labeled axons arborize in a diffuse manner predominantly within areas enriched with CaBP, AChE, or NADPH-diaphorase, representing the matrix compartment, and tend to avoid areas poor in these substances, corresponding to the patch/striosome compartment. In the sensorimotor territory labeled axons form bands that occupy a subregion of the NADPH-diaphorase-rich zone in the putamen. The terminal pattern of the CM-striatal projection suggests the existence of a more complex mosaic organization within the sensorimotor territory. Ultrastructural analysis of PHA-L-labeled elements within the striatum reveals that both CM and Pf projections form asymmetric synapses upon dendrites and spines of striatal cells. A total of 339 PHA-L-labeled boutons were examined after CM injections and compared to 293 boutons following Pf injections. After CM injections, 29% of PHA-L-labeled terminals form synapses on dendritic spines and 66% on dendritic shafts, whereas after Pf injections only 12% of synapses occur on dendritic spines compared to 81% on dendritic shafts. Labeled terminals forming axosomatic or axoaxonic synapses were not seen within the striatum following either CM or Pf injections. It is concluded that in the squirrel monkey: 1) Pf-striatal fibers profusely arborize within the matrix compartment of the associative territory, 2) CM-striatal fibers form bands that occupy a subregion of the NADPH-diaphorase-rich zone within the sensorimotor territory, and 3) that both Pf- and CM-striatal projections establish asymmetric synapses with dendrites and spines of medium-sized spiny cells.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Efferent connections of the centromedian and parafascicular thalamic nuclei in the squirrel monkey: a light and electron microscopic study of the thalamostriatal projection in relation to striatal heterogeneity. 161 51

An antibody raised against the chick calcium-binding protein calbindin D28K was used in immunohistochemical studies of normal post mortem human brain and the brains of individuals with Huntington's disease. Calbindin D28K immunoreactivity in the caudate nucleus and putamen coincided with the distribution of areas of acetylcholinesterase staining termed the matrix. In the matrix, calbindin D28K immunoreactivity was present in medium-sized neurons, the major neuronal population, however a further minor population of more strongly stained large neurons was detected. In Huntington's disease there was a dramatic loss of the majority of matrix calbindin D28K immunoreactive neurons and a parallel loss of calbindin D28K immunoreactivity from the substantia nigra. In contrast to the medium-sized calbindin D28K immunoreactive neurons which degenerate in Huntington's disease, the larger immunoreactive neurons were relatively preserved.
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PMID:Calbindin D28K as a marker for the degeneration of the striatonigral pathway in Huntington's disease. 214 68

Immunoreactivity for two calcium binding proteins, 28 kDa calbindin and parvalbumin, was used to label cells morphologically identical to Cajal-Retzius neurons in the developing visual, prefrontal, sensory-motor and temporal cortex of Old World monkeys. At all fetal ages examined (E110-E155), Cajal-Retzius neurons throughout the cortex were immunoreactive for calbindin as well as being acetylcholinesterase positive. Between E130 and E150, the calbindin-immunoreactive Cajal-Retzius cells in the visual cortex, and a few in other cortical areas, also showed parvalbumin immunoreactivity. A reduced population of immunoreactive Cajal-Retzius cells was detected at birth, and none could be visualized by immunocytochemistry or histochemistry at later postnatal ages. Calbindin and parvalbumin immunoreactivity represents a potentially useful marker for this developmentally regulated population of neurons, and the varied expression of the two proteins suggests that Cajal-Retzius neurons may represent a neurochemically heterogeneous cell population.
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PMID:Cajal-Retzius neurons in developing monkey neocortex show immunoreactivity for calcium binding proteins. 235 29

Fetal striatal grafts display a striking modularity of composition. With acetylcholinesterase (AChE) histochemistry, the tissue of such grafts can be divided into regions with strong AChE staining of the neuropil and regions in which AChE staining of the neuropil is weak. In the experiments reported here, we reexamined the nature of this modularity. Striatal grafts were made by injecting dissociated cells of E15 ganglionic eminence into the striatum of adult rats, which 7 days before had recived intrastriatal deposits of ibotenic acid. Some donors had been exposed to 3H-thymidine at E11-E15. After 9-17 month survivals, the anatomical organization of the grafts was studied by histochemistry, immunohistochemistry, and autoradiography. In every graft, the AChE-rich regions formed patches (P regions) in a larger AChE-poor surround (NP regions). Neurons labeled with 3H-thymidine appeared in both P and NP regions, suggesting that donor cells were distributed in each type of region and that neither type of tissue, P or NP, was composed exclusively of host tissue. In the AChE-rich P regions, markers characteristic of normal perinatal and mature rat striatum were expressed by medium-sized cells: calcium-binding protein (calbindin D28k) immunostaining, metenkephalin (mENK) immunostaining, and, more rarely, somatostatin (SOM) immunostaining. In the NP regions, however, medium-sized cells expressing calbindin and mENK immunostaining were very rare, and there was an abundance of neuronal types not found in normal mature striatal tissue. These included (1) large, multipolar, calbindin-positive neurons with well-ramified, densely stained dendrites, (2) large, SOM-positive neurons with prominent dendritic trees, and (3) mENK-positive cells smaller than typical striatal, medium-sized, mENK-immunoreactive neurons. In Nissl stains, the AChE-rich P regions resembled the normal striatum of mature animals, whereas the AChE-poor NP regions did not. These findings suggest that the P regions of fetal striatal grafts achieve a phenotypy similar to that of normal striatum at maturity and during much of postnatal development. The dominant expression of perikaryal calbindin-like immunoreactivity in the P regions further suggests that these zones have a high proportion of tissue resembling striatal matrix. By contrast, expression of marker antigens in the NP zones of the grafts suggests that these zones are predominantly composed of nonstriatal tissue or that they have the phenotypy of immature striatum intermixed with some nonstriatal cells.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Intrastriatal grafts derived from fetal striatal primordia. I. Phenotypy and modular organization. 247 13

The orbital and medial prefrontal cortex (OMPFC) of macaque monkeys is a large but little understood region of the cerebral cortex. In this study the architectonic structure of the OMPFC was analyzed with nine histochemical and immunohistochemical stains in 32 individuals of three macaque species. The stains included Nissl, myelin, acetylcholinesterase, Timm, and selenide stains and immunohistochemical stains for parvalbumin, calbindin, a nonphosphorylated neurofilament epitope (with the SMI-32 antibody), and a membrane-bound glycoprotein (with the 8b3 antibody). In addition to patterns of cell bodies and myelinated fibers, these techniques allow the visualization of markers related to metabolism, synapses, and neurotransmitters. A cortical area was defined as distinct if it was differentiated in at least three different stains and, as described in later papers, possessed a distinct set of connections. Twenty-two areas were recognized in the OMPFC. Walker's areas 10, 11, 12, 13, and 14 [J. Comp. Neurol. (1940) 73:59-86] have been subdivided into areas 10m, 10o, 11m, 11l, 12r, 12l, 12m, 12o, 13m, 13l, 13a, 13b, 14r, and 14c. On the medial wall, areas 32, 25, and 24a,b,c have been delineated, in addition to area 10m. The agranular insula also has been recognized to extend onto the posterior orbital surface and has been subdivided into medial, intermediate, lateral, posteromedial, and posterolateral agranular insula areas. The OMPFC, therefore, resembles other areas of primate cortex, such as the posterior parietal and temporal cortices, where a large number of relatively small, structurally and connectionally distinct areas have been recognized. Just as the area-specific neurophysiological properties of these parietotemporal areas underlie broader regional functions such as visuospatial analysis, it is likely that the many small areas of the OMPFC also make differential contributions to the general mnemonic, sensory, and affective functions of this region.
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PMID:Architectonic subdivision of the orbital and medial prefrontal cortex in the macaque monkey. 752 5

Experiments were conducted to characterise the Fos-immunopositive neurons that are observed in the dorsal rim of the striatum following monoamine depletion by the systemic administration of reserpine. Using a retrograde tract-tracer, some of these neurons could be shown to project to the globus pallidus but none were seen to project to the entopeduncular nucleus. In addition, these neurons were located in a region of both poor calbindin immunoreactivity and cholinesterase activity. It can be concluded that Fos levels are increased only in a subset of striatopallidal neurons following monoamine depletion. This subset of neurons is located in the dorsal region of the striatum where it has previously been shown that neurons can preferentially be induced to undergo apoptosis upon monoamine depletion.
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PMID:A subset of striatopallidal neurons are Fos-immunopositive following acute monoamine depletion in the rat. 762 23

The distribution of vesicular or chelatable zinc was analysed in the dorsal and ventral subdivisions of the striatum and globus pallidus of the rat with Danscher's selenium method. Acetylcholinesterase and Calbindin-D28k were used as striatal and pallidal markers in order to analyse the possible compartmentalization of the distribution of zinc in the striatum and globus pallidus. The main findings of this study are the following: (1) The distribution of vesicular zinc in the dorsal striatum was heterogeneous. A peripheral rim of tissue heavily stained for zinc was detected in the medial, dorsal and lateral striatal areas, along most of the rostrocaudal extent of the striatum. addition, patch-like zones intensely stained for zinc were prominent in the rostral half of the caudate-putamen complex. (2) In some regions of the rostral half of the caudate-putamen complex, the staining for zinc appeared to follow the well-known striatal patches (striosomes)/matrix organization. However, in other regions of the rostral half of the striatum such a relation was not detected. (3) The ventral striatum also showed a heterogeneous staining for zinc. Thus, in the most ventral part of the caudate-putamen complex, both subdivisions of the nucleus accumbens and parts of the olfactory tubercle displayed different patterns of compartmentalized distribution of zinc. In the dorsal half of the shell of the nucleus accumbens, some patches with an intense reaction for zinc seemed to overlap with acetylcholinesterase-poor patches. (4) There was a remarkable absence of staining for zinc in the globus pallidus. This histochemical study illustrates, on the one hand, the high content of vesicular zinc in the dorsal and ventral subdivisions of the striatum, which was distributed following different patterns of chemical compartmentalization, and on the other hand, the absence of vesicular zinc in the globus pallidus of the rat.
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PMID:Heterogeneous and compartmental distribution of zinc in the striatum and globus pallidus of the rat. 764 17

The aim of this study was to examine how the functional specialization of the barn owl's auditory brainstem might correlate with histochemical compartmentalization. The barn owl uses interaural intensity and time differences to encode, respectively, the vertical and azimuthal positions of sound sources in space. These two auditory cues are processed in parallel ascending pathways that separate from each other at the level of the cochlear nuclei. Sections through the auditory brainstem were stained for acetylcholinesterase (AChE) to examine whether nuclei that process different auditory cues stain differentially for this enzyme. Of the two cochlear nuclei, angularis showed more intense staining than nucleus magnocellularis. Nucleus angularis projects to all of the nuclei and subdivisions of nuclei that belong to the intensity processing pathway. Acetylcholinesterase stained all regions that contain terminal fields of nucleus angularis and thus provided discrimination between the time and intensity pathways. Moreover, staining patterns with acetylcholinesterase were complementary to those previously reported with an anti-calbindin antibody, which stains terminal fields of nucleus laminaris, and thus stains all the nuclei and subdivisions of nuclei that belong to the time pathway. Some of the gross staining patterns observed with AChE were similar to those reported with antibodies to glutamate decarboxylase. However, AChE is a more convenient and definitive marker in discriminating between these pathways than is calbindin or glutamate decarboxylase. Acetylcholinesterase staining of the intensity pathway in the owl may be related to encoding of sound intensity by spike rate over large dynamic ranges.
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PMID:Acetylcholinesterase staining differentiates functionally distinct auditory pathways in the barn owl. 768 56

The effect of prenatal cocaine on the anatomical development of the striatum was examined. The distribution and density of dopaminergic innervation of the striatum of animals exposed to cocaine during the second and third week of gestation was not noticeably different from prenatally saline-injected or untreated controls at any age. The patch/matrix organization of the striatum also appeared unaltered: neurons exhibiting dense substance P staining were localized to patches that overlapped dopamine terminal patches early in development, and enkephalin- and calbindin-immunoreactive neurons were found segregated to the matrix. Histochemical staining for acetylcholinesterase and NADPH diaphorase also revealed no differences between prenatally cocaine-treated and control brains. Whereas prenatal cocaine treatment failed to modify the basic compartmental organization of the striatum, it did lead to a hyperinnervation of serotonin-immunoreactive fibers which developed slowly after birth. Thus prenatal exposure to cocaine is capable of altering the ingrowth of serotonergic projections to the striatum while producing no change in the organization of neurons intrinsic to the striatum.
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PMID:Prenatal cocaine increases striatal serotonin innervation without altering the patch/matrix organization of intrinsic cell types. 769 34

A competitive antagonist of the N-methyl-D-aspartate receptor, CGP 39551, was administered daily to neonatal rats with increasing doses from postnatal day 1 to 22. These animals displayed approximately 50% decrease of body weight at the end of treatment and, therefore, both normal and neonatally undernourished rats were used as controls. At a young adult stage (55-75 days of age) CGP 39551-treated rats showed a much higher spontaneous locomotor activity as compared to control groups. This hypermotility was counteracted by D1 and D2 dopamine antagonists while administration of methamphetamine increased, to the same extent, the differential basal locomotor activity of treated and control groups. The locomotor activity response to the N-methyl-D-aspartate channel blocker, dizocilpine maleate, was significantly shifted to the right for treated rats so that an equivalent increase of motility was obtained by doubling the dose effective for control animals. In in vivo microdialysis experiments, similar amounts of dopamine were collected from the striatum of treated and control rats after high K+ or methamphetamine stimulation, the only difference being a greater Ca2+ dependency of the depolarization-induced dopamine release in treated rats. Assays for different neurochemical parameters, carried out at 80-90 days of age, suggested some alteration of the balance between excitatory and inhibitory circuits in the basal ganglia of CGP 39551-treated rats. Tyrosine hydroxylase and calbindin immunostaining, as well as acetylcholinesterase histochemistry, revealed a similar picture in the striatum of treated and control rats. However, 5'-nucleotidase histochemistry showed a stronger and evenly distributed reactivity in the striatum of treated rats, opposite to the weaker and patchy localization of normal or undernourished controls. From the present results it is possible to conclude that chronic blockade of the N-methyl-D-aspartate receptor during neonatal brain maturation results in long-lasting alteration of locomotor activity which appears related to functional changes of the dopamine receptors as well as to an altered balance between various excitatory and inhibitory neurotransmitter and neuromodulatory systems.
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PMID:Long-lasting effects of chronic neonatal blockade of N-methyl-D-aspartate receptor through the competitive antagonist CGP 39551 in rats. 791 9


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